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2_test

{"project":"2_test","denotations":[{"id":"20150961-11898581-67933695","span":{"begin":262,"end":263},"obj":"11898581"},{"id":"20150961-15845210-67933696","span":{"begin":485,"end":486},"obj":"15845210"},{"id":"20150961-10963608-67933697","span":{"begin":841,"end":842},"obj":"10963608"},{"id":"20150961-10679407-67933698","span":{"begin":999,"end":1000},"obj":"10679407"},{"id":"20150961-11477402-67933699","span":{"begin":1002,"end":1003},"obj":"11477402"},{"id":"20150961-10679407-67933700","span":{"begin":1307,"end":1308},"obj":"10679407"},{"id":"20150961-11477402-67933701","span":{"begin":1310,"end":1311},"obj":"11477402"},{"id":"20150961-17884182-67933702","span":{"begin":1519,"end":1520},"obj":"17884182"},{"id":"20150961-17884182-67933703","span":{"begin":1749,"end":1750},"obj":"17884182"},{"id":"20150961-17372179-67933704","span":{"begin":1752,"end":1753},"obj":"17372179"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

pmc-enju-pas

bionlp-st-ge-2016-test-proteins

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T867","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T866","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T865","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T864","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T863","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T862","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T861","span":{"begin":1068,"end":1072},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

bionlp-st-ge-2016-uniprot

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T1656","span":{"begin":2093,"end":2097},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T1655","span":{"begin":2042,"end":2046},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T1654","span":{"begin":1903,"end":1907},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T1653","span":{"begin":1871,"end":1875},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T1652","span":{"begin":1787,"end":1791},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T1651","span":{"begin":1563,"end":1567},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T1650","span":{"begin":1068,"end":1072},"obj":"http://www.uniprot.org/uniprot/O00206"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T837","span":{"begin":1640,"end":1659},"obj":"http://purl.obolibrary.org/obo/UBERON_0000120"},{"id":"T836","span":{"begin":1640,"end":1645},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T835","span":{"begin":2130,"end":2136},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T834","span":{"begin":417,"end":423},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T833","span":{"begin":281,"end":287},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T832","span":{"begin":2124,"end":2129},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T831","span":{"begin":1799,"end":1804},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T830","span":{"begin":1715,"end":1720},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T829","span":{"begin":1668,"end":1673},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T828","span":{"begin":1646,"end":1651},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T827","span":{"begin":1502,"end":1507},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T826","span":{"begin":613,"end":618},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T825","span":{"begin":457,"end":462},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T824","span":{"begin":411,"end":416},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T823","span":{"begin":316,"end":321},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T822","span":{"begin":275,"end":280},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T883","span":{"begin":1633,"end":1638},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T882","span":{"begin":1085,"end":1100},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T881","span":{"begin":1854,"end":1867},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T880","span":{"begin":1249,"end":1262},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T879","span":{"begin":918,"end":931},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T878","span":{"begin":817,"end":829},"obj":"http://purl.obolibrary.org/obo/GO_0009293"},{"id":"T877","span":{"begin":810,"end":829},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T876","span":{"begin":2107,"end":2116},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T875","span":{"begin":1917,"end":1926},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T874","span":{"begin":884,"end":893},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T873","span":{"begin":810,"end":816},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T872","span":{"begin":950,"end":962},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T871","span":{"begin":1374,"end":1396},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T870","span":{"begin":1283,"end":1305},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T869","span":{"begin":671,"end":693},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T868","span":{"begin":381,"end":403},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

GO-MF

{"project":"GO-MF","denotations":[{"id":"T887","span":{"begin":1042,"end":1048},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T890","span":{"begin":1209,"end":1216},"obj":"http://purl.obolibrary.org/obo/GO_0005634"},{"id":"T889","span":{"begin":776,"end":789},"obj":"http://purl.obolibrary.org/obo/GO_0044214"},{"id":"T888","span":{"begin":776,"end":789},"obj":"http://purl.obolibrary.org/obo/GO_0016021"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

sentences

ICD10

{"project":"ICD10","denotations":[{"id":"T886","span":{"begin":1721,"end":1727},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T885","span":{"begin":1508,"end":1514},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T884","span":{"begin":619,"end":625},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

simple1

{"project":"simple1","denotations":[{"id":"T930","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T929","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T928","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T927","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T926","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T925","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T924","span":{"begin":1068,"end":1072},"obj":"Protein"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

BioNLP16_DUT

{"project":"BioNLP16_DUT","denotations":[{"id":"T1722","span":{"begin":1854,"end":1867},"obj":"Transcription"},{"id":"T1721","span":{"begin":1593,"end":1603},"obj":"Binding"},{"id":"T1720","span":{"begin":1073,"end":1080},"obj":"Positive_regulation"},{"id":"T1719","span":{"begin":1054,"end":1064},"obj":"Positive_regulation"},{"id":"T1718","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T1717","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T1716","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T1715","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T1714","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T1713","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T1712","span":{"begin":1068,"end":1072},"obj":"Protein"}],"relations":[{"id":"R1310","pred":"themeOf","subj":"T1712","obj":"T1719"},{"id":"R1311","pred":"themeOf","subj":"T1713","obj":"T1721"},{"id":"R1312","pred":"themeOf","subj":"T1715","obj":"T1722"},{"id":"R1313","pred":"themeOf","subj":"T1719","obj":"T1720"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

BioNLP16_Messiy

{"project":"BioNLP16_Messiy","denotations":[{"id":"T1665","span":{"begin":1854,"end":1867},"obj":"Transcription"},{"id":"T1664","span":{"begin":1054,"end":1064},"obj":"Positive_regulation"},{"id":"T1663","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T1662","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T1661","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T1660","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T1659","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T1658","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T1657","span":{"begin":1068,"end":1072},"obj":"Protein"}],"relations":[{"id":"R1289","pred":"themeOf","subj":"T1657","obj":"T1664"},{"id":"R1290","pred":"themeOf","subj":"T1660","obj":"T1665"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

DLUT931

{"project":"DLUT931","denotations":[{"id":"T1675","span":{"begin":1854,"end":1867},"obj":"Transcription"},{"id":"T1674","span":{"begin":1135,"end":1146},"obj":"Binding"},{"id":"T1673","span":{"begin":1054,"end":1064},"obj":"Positive_regulation"},{"id":"T1672","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T1671","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T1670","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T1669","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T1668","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T1667","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T1666","span":{"begin":1068,"end":1072},"obj":"Protein"}],"relations":[{"id":"R1291","pred":"themeOf","subj":"T1666","obj":"T1673"},{"id":"R1292","pred":"themeOf","subj":"T1666","obj":"T1674"},{"id":"R1293","pred":"themeOf","subj":"T1669","obj":"T1675"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

bionlp-st-ge-2016-test-ihmc

bionlp-st-ge-2016-spacy-parsed

bionlp-st-ge-2016-test-tees

testone

{"project":"testone","denotations":[{"id":"T804","span":{"begin":1854,"end":1867},"obj":"Transcription"},{"id":"T803","span":{"begin":1054,"end":1064},"obj":"Positive_regulation"},{"id":"T802","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T801","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T800","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T799","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T798","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T797","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T796","span":{"begin":1068,"end":1072},"obj":"Protein"}],"relations":[{"id":"R542","pred":"themeOf","subj":"T796","obj":"T803"},{"id":"R543","pred":"themeOf","subj":"T799","obj":"T804"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

test3

{"project":"test3","denotations":[{"id":"T821","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T820","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T819","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T818","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T817","span":{"begin":1854,"end":1867},"obj":"Transcription"},{"id":"T816","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T815","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T814","span":{"begin":1073,"end":1080},"obj":"Positive_regulation"},{"id":"T813","span":{"begin":1068,"end":1072},"obj":"Protein"},{"id":"T812","span":{"begin":424,"end":431},"obj":"Positive_regulation"},{"id":"T811","span":{"begin":2093,"end":2097},"obj":"Protein"},{"id":"T810","span":{"begin":2042,"end":2046},"obj":"Protein"},{"id":"T809","span":{"begin":1903,"end":1907},"obj":"Protein"},{"id":"T808","span":{"begin":1871,"end":1875},"obj":"Protein"},{"id":"T807","span":{"begin":1787,"end":1791},"obj":"Protein"},{"id":"T806","span":{"begin":1563,"end":1567},"obj":"Protein"},{"id":"T805","span":{"begin":1068,"end":1072},"obj":"Protein"}],"relations":[{"id":"R544","pred":"themeOf","subj":"T818","obj":"T817"}],"text":"1. Introduction\nIntracerebral hemorrhage (ICH) represents 10%–15% of all strokes and occurs with increasing frequency as a complication of the thrombolytic treatment of ischemic stroke, which is associated with high mortality and severe disability in survivors [1, 2]. Local brain tissue deformation induces primary brain damage after ICH; more importantly, the excitotoxicity and inflammatory responses in the brain tissue induced by ICH result in further brain damage following ICH [3]. Both innate and adaptive immunological/inflammatory mechanisms have been clearly shown to participate in the progression of brain injury after ischemic stroke. Nevertheless, how the inflammatory responses in ICH are triggered and regulated remains to be elucidated.\nTLRs are a family of transmembrane proteins and act as signal transduction molecules [4]. Activation of TLRs recruits downstream signaling proteins and results in transcription of genes encoding inflammation-associated molecules and cytokines [5, 6]. For example, combined with specific ligand, the activation of TLR4 induces the phosphorylation of inhibitor of kappa-B (IκB) and dissociates IκB from NF-kappa-B (NFκB). Then, NFκB trans-locates into the nucleus and activates and regulates the transcription of genes related to inflammatory responses [5, 6]. TLRs play a critical role in the induction of immunological/inflammatory responses and are implicated in several CNS diseases, such as infectious disease, autoimmune disease, and ischemic brain injury [7, 8]. Accumulating evidences demonstrate that TLR4, the first mammalian TLR recognized, contributes to the neuronal death, blood brain barrier damage, brain edema, and inflammatory responses in the brain injury induced by ischemia [8, 9]. However, little is known about TLR4 in the brain after ICH. In the present study, we detected the transcription of TLR4 gene and the activation of TLR4-mediated signaling in the rat brains subjected to experimental ICH. Our data firstly provided the knowledge about the distribution of TLR4 and the temporal profile of the activation of TLR4-mediated signaling in rat brain tissue after ICH."}

PMC:2817507 / 1381-3528 JSONTXT

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PMC:2817507 / 1381-3528 JSON TXT